The big picture: Uric acid is a chemical created when your body breaks down substances called purines. Too much uric acid can lead to gout and kidney stones, and chronically elevated uric acid is a biomarker for chronic disease, including chronic kidney disease, cardiovascular disease and type 2 diabetes.

Purine, an essential chemical for DNA and RNA synthesis, is primarily obtained from food, and when processed creates uric acid.

About one-third of purines enter the body through food. The rest are either produced by the body or get released into the bloodstream when cells die.
When purines are processed in the body, they create a byproduct called uric acid.
Normally, about 90% of uric acid is recycled into the body, and the rest is removed via the kidney and the gut: around 70% as urine and around 30% as stool.
A diet rich in animal sources of protein, yeast in beer, and fructose can increase uric acid levels. However, genetics may play the most significant role in determining uric acid levels. Despite removing all known factors that affect uric acid metabolism, levels in some individuals remain elevated, which can indicate a genetic predisposition.

About 1 in 5 people in the United States suffer from hyperuricemia, an excess level of uric acid in the bloodstream. This can occur when the body produces too much uric acid, when dietary intake is too high in purines, or when the kidneys are unable to eliminate it efficiently.

There is growing evidence there is a bi-directional relationship between uric acid and insulin resistance.

Insulin helps the body to remove uric acid from the blood. When insulin resistance is present, the body is not able to effectively remove uric acid, leading to elevated levels.
Studies have also shown that high uric acid levels can contribute to insulin resistance and diabetes by interfering with the action of insulin, inducing oxidative stress (cell damage), and reducing the production of important hormones involved in regulating blood sugar levels
Reducing uric acid levels has been found to improve insulin resistance in animal models of metabolic syndrome. In human studies, the evidence is limited, but some medications that lower uric acid levels have shown potential benefits in improving insulin resistance and blood sugar control in people with diabetes.

Hyperuricemia can lead to an inflammatory arthritis called gout and kidney stones.

Gout occurs when uric acid crystals settle in the joints and cause an inflammatory reaction leading to redness, swelling and agonizing pain. The symptoms typically appear suddenly, overnight.
When uric acid crystals form, they can collect in the kidney and cause kidney stones. There are different types of kidney stones; uric acid stones are just one type.

Hyperuricemia also increases your risk for heart disease and heart failure by up to 65%.

One meta-analysis (n=427,917) showed that hyperuricemia was associated with a 65% increased risk in heart failure and 45% increased in risk of death by heart failure.
Further, for every 1 mg/dL increase in uric acid, the odds of development of heart failure increased by 19%, the risk of death by heart failure increased by 28%.
Another meta-analysis (n=341,389) found that for every 1 mg/dL of uric acid above normal, individuals had a 20% increased risk of developing coronary heart disease, 14% increased risk for death by coronary heart disease and 9% increased risk for all-cause mortality